A mutation that seems trivial could be making the virus spread more easily.
Health-care workers from University of South Florida Health administer coronavirus testing June 25 at a community center in Tampa. By Sarah Kaplan and Sarah Kaplan Climate and science reporter Email Bio Follow Joel Achenbach Joel Achenbach Reporter covering science and politics Email Bio June 29 at 9:00 AM When the first coronavirus cases in Chicago appeared in January, they bore the same genetic signatures as a germ that emerged in China weeks before.
But the location was significant, because the switch occurred in the part of the genome that codes for the all-important “spike protein” — the protruding structure that gives the coronavirus its crownlike profile and allows it to enter human cells the way a burglar picks a lock.And its ubiquity is undeniable.
“The epidemiological study and our data together really explain why the [G variant’s] spread in Europe and the U.S. was really fast,” said Hyeryun Choe, a virologist at Scripps Research and a lead author of an unpublished study on the G variant’s enhanced infectiousness in laboratory cell cultures. “This is not just accidental.”
A mutation in the spike protein of the SARS-CoV-2 virus changes just one amino acid in a chain of about 1,300, but it might make a difference in how the virus attacks human cells. The mutation , which first appeared in January, is found in what has become the dominant variant of the coronavirus.Proportion of samples with the D614G mutation0.
The spike protein for SARS-CoV-2 has two parts that don’t always hold together well. In the version of the virus that arose in China, Choe said, the outer part — which the virus needs to attach to a human receptor — frequently broke off. Equipped with this faulty lock pick, the virus had a harder time invading host cells.
Neville Sanjana, a geneticist at the New York Genome Center and New York University, was trying to figure out which genes enable SARS-CoV-2 to infiltrate human cells. But in experiments based on a gene sequence taken from an early case of the virus in Wuhan, he struggled to get that form of the virus to infect cells. Then the team switched to a model virus based on the G variant.
Luban, who has also been experimenting with the D614G mutation, has been drawn to a third possibility: His experiments suggest that the mutation allows the spike protein to change shape as it attaches to the ACE2 receptor, improving its ability to fuse to the host cell. Cell culture experiments have been wrong before, noted Anderson Brito, a computational biologist at Yale University. Early experiments with hydroxychloroquine, a malaria drug, hinted that it was effective at fighting the coronavirus in a petri dish. The drug was touted by President Trump, and the Food and Drug Administration authorized it for emergency use in hospitalized covid-19 patients.
The Los Alamos draft drew intense scrutiny when it was released in the spring, and many researchers remain skeptical of its conclusions.
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